Background: Although nonsustained ventricular tachycardia (NSVT) is a risk factor for sudden cardiac death in hypertrophic-cardiomyopathy (HCM), the impact of premature ventricular contraction (PVC) burden, in the absence of NSVT, is not well-known. Hypothesis: PVC burden may be associated with myocardial fibrosis and genetic mutations in patients with HCM. Methods: Of the 212 patients prospectively enrolled to the HCM registry of genetics, 84 were evaluated with both cardiac magnetic resonance, 24-hour Holter monitoring and genetic analysis. Among them, 71 patients have not been diagnosed with NSVT. Results: Patients with NSVT (n = 13) had a higher late gadolinium enhancement (LGE) amount, extracellular volume fraction (ECV), and prevalence of sarcomere mutations compared with patients without NSVT. Among patients without NSVT, those with LGE (n = 46) had a higher total PVC (109 ± 332 vs 7 ± 13, P =.003) and PVC burden (0.114 ± 0.225 vs 0.008 ± 0.014%, P =.003) during 24-hour Holter monitoring compared with others. The %LGE and global ECV were correlated with PVC burden (r = 0.377, P =.001; r = 0.401, P =.001). The optimal cutoff value for PVC number for LGE was 45 (37.0% and 100% sensitivity and specificity, respectively) with 0.733 of the area under the receiver operating characteristic-curve (P <.001). Thick filament gene mutation was more prevalent in the higher PVC burden group (41.2% vs 16.7%, P =.048). Conclusion: Total PVC burden is significantly related to increase in myocardial fibrosis in HCM patients without NSVT.
Bibliographical noteFunding Information:
National Research Foundation of Korea, Grant/Award Number: 2014R1A1A2055872 Funding information
This work was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education. (2014R1A1A2055872).
© 2020 The Authors. Clinical Cardiology published by Wiley Periodicals LLC.
All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine